Any discussion of the prior art throughout the specification should in no way be considered as an admission that such prior art is widely known or forms part of common general knowledge in the field.
In myocardial fibrosis, heart muscle is replaced by fibrous or scar tissue. This can interfere with the flexibility of the heart muscle. It can lead to a decrease in function and, eventually, to overt heart failure. Use of VIP and certain fragments of VIP in therapeutic and prophylactic treatment of myocardial fibrosis and related conditions was described in PCT/AU2005/000835, incorporated in its entirety herein by reference.
Conventional view of structure/function relationship with respect to VIP activity is that the N-terminal amino acid residues (1-5) are important and necessary for signal delivery once VIP binds to its receptor. Further, there are certain key amino acid residues throughout the VIP molecule, distal to the N-terminus, that are important for receptor binding. This would suggest that fragments of VIP lacking either the N-terminal residues or significant portions that encompass the receptor binding residues would not be fully functional. Earlier studies with two VIP fragments, described in PCT/AU2005/000835, indicate that such fragments of VIP could be active, at least in the treatment of myocardial fibrosis.
It is an object of the present invention to identify additional fragments of VIP that are active in the treatment of conditions such as myocardial fibrosis, that would overcome certain disadvantages associated with using the entire VIP molecule or large portions thereof, or at least provide a useful alternative.